Circ_0044411 silencing protects infantile pneumonia from lipopolysaccharide-induced cell injury by sponging miR-141-3p to inhibit CCL16 expression.

Abstract

Circular RNA (circRNA) has been found to play an important role in the progression of many diseases, including infantile pneumonia. However, the role of circ_0044411 in infantile pneumonia progression is still unclear. MRC-5 cells were incubated with lipopolysaccharide (LPS) for 12h to establish the in vitro cellular model for infantile pneumonia. Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) was used to detect the levels of circ_0044411, miR-141-3p (micoRNA-141-3p) and CCL16 (CC motif chemokine ligand 16). Cell viability and proliferation was assessed by 3-(4, 5-dimethylthiazol-2-y1)-2, 5-diphenyl tetrazolium bromide (MTT) assay and 5-ethynyl-2'-deoxyuridine (EdU) assay. The levels of inflammatory factors IL-1β, IL-6 and TNF-α were determined by enzyme-linked immunosorbent assay kits. Cell apoptosis and caspase-3 activity were detected by flow cytometry analysis and caspase-3 activity assay kit. The target interaction was confirmed by dual-luciferase reporter assay, RNA immunoprecipitation assay and RNA pull-down assay. Circ_0044411 was highly repressed in the serum of infantile pneumonia patients and LPS-induced MRC-5 cells. Circ_0044411 could promote the cell viability and proliferation, inhibit inflammatory response and apoptosis in LPS-induced MRC-5 cells. Circ_0044411 could serve as a sponge of miR-141-3p, and miR-141-3p could reverse the function of circ_0044411 on LPS-induced MRC-5 cell injury. In addition, miR-141-3p could target CCL16, and miR-141-3p could protect MRC-5 cells from LPS-induced cell injury by targeting CCL16. Furthermore, circ_0044411 sponged miR-141-3p to positively regulate CCL16 expression. Circ_0044411 knockdown promoted cell viability and proliferation, inhibited inflammatory response and apoptosis by regulating miR-141-3p/CCL16 axis, indicating that circ_0044411 might be a potential therapeutic target for IP.